The research focuses on the nature of the stimuli that might control the cardiovascular system during exercise. Our general hypothesis is that centrally generated motor signals (central command) set basic patterns of effector activity which in turn are modulated by baroreceptors and by chemosensitive (muscle "chemosensors") and mechanosensitive nerves in muscle. We propose to examine how effectively a skeletal muscle chemo-reflex might serve to restore working muscle blood flow (MBF) by raising blood pressure (BP) in response to graded partial terminal aortic occlusions. We also will raise and lower total cardiac output during exercise in the heart-blocked dog with a chronically implanted ventricular pacing electrode - and examine BP responses on both the up and down side of changing total MBF. We are asking (1) What is the "gain" of this pressure-raising reflex before and after cervical sino-aortic denervation of baroreceptors? (2) Are the pressor responses opposed by baroreflexes? (3) Are the pressor responses well correlated with femoral venous P02 levels and with increments in certain metabolites? (4) Do reflexes from under-perfused working muscle augment vasoconstrictor outflow to visceral organs? (5) Does the reflex have a well-defined threshold below which only central command might operate? We hypothesize that central command activates in parallel bvoth locomotor and cardiovascular systems. Use of selective neuromuscular blockade will help us to test whether cardiovascular responses are a function of motor unit recruitment in muscle. We will study responses to static exercise in baboons and dynamic exercise in dogs with and without partial circulatory occlusion before and after lesions in a subthalamic region known to elicit circulatory responses. In this way we should be able to separate and identify a role of central vs. peripheral signals. The experimens provide a new approach to investigation of central and peripheral factors controlling the circulation of conscious animals during exercise.